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trauma from occlusion

This document discusses trauma from occlusion (TFO), which refers to pathologic alterations or adaptive changes in the periodontium resulting from excessive occlusal forces. It covers the historical understanding of TFO, definitions, classifications, clinical features, and the periodontal response and adaptation to excessive forces. It also examines Glickman's concept of co-destruction between TFO and plaque-associated periodontal disease. The document provides details on injury, repair, remodeling processes in the periodontium in response to TFO.

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TRAUMA FROM OCCLUSION
CONTENTS  INTRODUCTION  HISTORICAL ASPECTS  DEFINITIONS  CLASSIFICATION  CLINICAL FEATURES  PERIODONTAL RESPONSE TO EXCESSIVE OCCLUSAL FORCES   INJURY  REPAIR  ADAPTIVE REMODELLING OF THE PERIODONTIUM  TRAUMA FROM OCCLUSION AND PLAQUE-ASSOCIATED PERIODONTAL DISEASE  GLICKMANS’ CONCEPT (THEORY OF CO-DESTRUCTION) WAERHAUG CONCEPT  CLINICAL TRIALS  HUMAN TRIALS  ANIMAL TRIALS  TFO AROUND IMPLANTS  PATHOLOGICAL TOOTH MIGRATION  EFFECT OF TFO ON DENTAL PULP  EFFECETS OF INSUFFICIENT OCCLUSAL FORCES  REVERSIBILITY OF TRAUMATIC LESIONS  LITERATURE REVIEWS  DIAGNOSIS  TREATMENT ASPECTS  CONCLUSION  REFERENCES
INTRODUCTION  For many years, the role of occlusion and its dynamic interactive impact on the periodontium has been an issue of controversy and extensive debate. Although a variety of occlusal conditions have purportedly been related to this interaction, the central focus has been on occlusal trauma resulting from excessive forces applied to the periodontium  Trauma from occlusion is a term used to describe pathologic alterations or adaptive changes which develop in the periodontium as a result of undue force produced by the masticatory muscles.  Trauma from occlusion is only one of many terms that have been used to describe such alterations in the periodontium.  In addition to producing damage in the periodontal tissues, excessive occlusal force may also cause injury in, for example, the temporomandibular joint, the masticatory muscles, and the pulp tissue.
HISTORICAL ASPECT 4 Karolyi (1901) – Postulated interaction between TFO & “alveolar pyrrohea” Stillman (1917 & 1926) – Advocated use of occlusal adjustment for treatment of TFO Box & Stones (1930’s ) - Animal experiments TFO etiologic factor in periodontal disease Orban & Weinman (1933) - Occlusal forces did not have a major effect on periodontal destruction. Glickman and co- workers (1960s ) - Performed a series of animal model and human autopsy studies Goldman et al in an experimental animal study, evaluated the effects of occlusal trauma on gingival blood flow. Stahl (1968) – Evaluated the interaction between occlusal trauma and plaque-induced periodontal inflammation. Waerhaug (1979)- Evaluated the relationship of the morphology of the bone & pocket with the plaque level and presence or absence of excessive occlusal forces.
DEFINITIONS 5 Other terms often used are: traumatizing occlusion, occlusal trauma, traumatogenic occlusion, periodontal traumatism, overload, etc.  STILLMANN “a condition where injury results to the supporting structures of the teeth by the act of bringing the jaws into a closed position When occlusal forces exceed the adaptive capacity of the tissues, tissue injury results.this resultant injury is termed TFO. (Glickman) STILLMANN “a condition where injury results to the supporting structures of the teeth by the act of bringing the jaws into a closed position Damage in the periodontium caused by stress on the teeth produced directly or indirectly by teeth of the opposing jaw. (WHO,1978) An injury to the attachment apparatus as a result of excessive occlusal force. (Glossary of periodontic terms AAP,1992)
CLASSIFICATION 6  Glickman’s classification (1953)  According to duration of cause:  i. Acute TFO  ii. Chronic TFO.  According to nature of cause:  i. Primary TFO  ii. Secondary TFO.  Box’s classification  Physiologic occlusion Box defined it as a condition, in which the systems of forces acting upon the tooth during the occlusion are in a state of equilibrium, and they do not and cannot change the normal relationship existing between the tooth and its supporting structures.  Traumatic occlusion The damage produced in the periodontium is due to the overstress produced by the occlusion
7 •Acute Trauma •Occurs on abrupt occlusal impact. •Caused by restorations or prosthetic appliances that interfere with or alter the direction of occlusal forces on the teeth. •Results in tooth pain, sensitivity to percussion and increased tooth mobility ACUTE TRAUMA •Chronic Trauma •It is more common than acute and is of greater clinical significance. •Caused by gradual changes in the occlusion produced by tooth wear, drifting movement and extrusion of teeth combined with para- functional habits such as bruxism and clenching. CHRONIC TRAUMA
8 When trauma to the supporting tissues occurs as a result of alterations in occlusal forces, it is called primary TFO. •High filling •Prosthetic replacement creating excessive forces •Drifting or extrusion of teeth •Orthodontic movement into functionally unacceptable oppositions In primary TFO there are no changes in the level of connective tissue attachment and no pocket formation Secondary TFO Occurs when, the adaptive capacity of the tissues to withstand occlusal forces is impaired by bone loss resulting from marginal inflammation.  This reduces the periodontal attachment area and alters the leverage on the remaining tissues.  The periodontium becomes vulnerable to injury, and previously well tolerated forces become traumatic.  Combined occlusal trauma refers to injury resulting from abnormal occlusal forces applied to a tooth or teeth with inadequate (abnormal) periodontal support
9  1. Normal periodontium with normal height of bone  2. Normal periodontium with reduced height of bone  3. Marginal periodontitis with reduced height of bone  It has been found in experimental animals that systemic disorders can reduce tissue resistance and that previously tolerable forces may become excessive. This could theoretically represent another mechanism by which tissue resistance to increased forces is lowered, thereby resulting in secondary trauma from occlusion
The signs and symptoms of chronic trauma from occlusion include (AAP, 2000).10  Tooth mobility  Tooth migration  Tooth pain or discomfort on chewing or percussion  Widening of the PDL, disruption of the lamina dura, radiolucency in the furcation or at the apex of vital teeth, root resorption as observed in intra-oral X-rays images  Tenderness of mastication muscles and/or TMJ dysfunction  Presence of wear facets beyond levels expected for patient’s age or diet  Chipped enamel or crown/root factures  Increased width of periodontal ligament space, often with thickening of the lamina dura along the lateral aspect of the root, in the apical and furcation areas,  Angular bone loss, mainly at the coronal level of interdental septum, with a funnel-shaped morphology  Radiolucency lamina dura surrounding the angular bone loss, resembling an infrabony defect  Condensation of the alveolar bone can be produced after widening of the periodontal ligament  Root resorption
INFLUENCE OF OCCLUSION ON THE PERIODONTIUM11  CLINICAL FEATURES  Progressive mobility  Fremitus  Wear facets  Occlusal discrepencies  Fractured tooth  Thermal sensivity
12  Fremitus is a measurement of the vibratory patterns of the teeth when the teeth are placed in contacting positions and movements.  A dampened index finger is placed along the buccal and labial surfaces of the maxillary teeth, and patient is asked to tap the teeth together in the maximum ICP and grind systemically in the lateral, protrusive, and lateral protrusive contacting movements and positions  • Class 1: Mild vibration or movement detected  • Class II: Easily palpable vibration but no visible movement  • Class III: Movement visible with the naked eye.
Radiographic features 13  Increased width of the periodontal space, often with thickening of the lamina dura along the lateral aspect of the root, in the apical region, and in the bifurcation areas.  A vertical destruction of the interdental septum  Root resorption.  Lipping
Gingival recession?? 14  Although it has been speculated that the elimination of trauma by occlusal adjustment, relieving the incidence of excessive occlusal force on teeth showing gingival cleft formation, resulted in spontaneous remission of gingival recession, with no additional treatment performed  Furthermore, no relationship was found between the existence of occlusal discrepancies, whether treated or not, and changes in keratinized gingiva width, as described by Harrel and Nunn  A recent systematic review to investigate the role of traumatic occlusion in the initiation and progression of gingival recessions was performed, in an attempt to gain a clearer understanding of the role of occlusion in these lesions  It could be concluded that the relationship between the conditions remains as “a clinical opinion” and that it seemed convenient to control occlusal factor in clinical practice because it can be considered as an independent risk factor for periodontal disease
ADAPTIVE CAPACITY OF THE PERIODONTIUM TO OCCLUSAL FORCES 15 Magnitude : When occlusal force is increased, the periodontium a thickening of the periodontal ligament, an increase in the number and width of the PDL fibers an increase in the density of alveolar bone. 2. Direction : reorientation of the stresses and strains The principal fibers of the PDL are arranged so that they best accommodate occlusal forces along the axis of the tooth . Lateral (horizontal) & torque (rotational) forces more injurious 3. Duration : Constant pressure Intermittent force 4 . Frequency more frequent
PERIODONTAL RESPONSE TO EXCESSIVE OCCLUSAL FORCES 16  Tissue response occurs in three stages:  Injury  Repair and  Adaptive remodeling of the periodontium
Tissue injury 17  Tissue injury is produced by excessive occlusal forces. The body then attempts to repair the injury and restore the periodontium.  This can occur if the forces are diminished or if the tooth drifts away from them. If the offending force is chronic, however, the periodontium is remodeled to cushion its impact.  The ligament is widened at the expense of the bone, which results in angular bone defects without periodontal pockets, and the tooth becomes loose.
18  Under the forces of occlusion, a tooth rotates around a fulcrum or axis of rotation, which in single-rooted teeth is located in the junction between the middle third and the apical third of the clinical root and in multirooted teeth in the middle of the interradicular bone .  This creates areas of pressure and tension on opposite sides of the fulcrum.  Different lesions are produced by different degrees of pressure and tension. If jiggling forces are exerted, these different lesions may coexist in the same area.
19  Slightly excessive pressure stimulates resorption of the alveolar bone, with a resultant widening of the periodontal ligament space.  Slightly excessive tension causes elongation of the periodontal ligament fibers and the apposition of alveolar bone.  In areas of increased pressure, the blood vessels are numerous and reduced in size; in areas of increased tension, they are enlarged.
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23  The areas of the periodontium that are most susceptible to injury from excessive occlusal forces are the furcations.  Injury to the periodontium produces a temporary depression in mitotic activity, in the rate of proliferation and differentiation of fibroblasts,in collagen formation, and in bone formation  These return to normal levels after the dissipation of the forces.
ORTHODONTIC TYPE TRAUMA 24  When a tooth is exposed to unilateral forces of a magnitude, frequency or duration that its periodontal tissues are unable to withstand and distribute while maintaining stability of the tooth, certain well-defined reactions develop in the periodontal structures to the altered functional demand  When horizontally directed forces are applied, the tooth tilts in direction of the force resulting in the development of pressure and tension zones within the marginal and apical parts the tooth becomes hypermobile temporarily, moves to a new position and healing takes place.  If the crown of the tooth is effected by such horizontally directed forces, eventually results in adaptation of periodontal structures to functional demand.  In this tissue reaction, bone resorbing osteoclasts soon appear on the bone surface of the alveolus in the pressure zone. A process of bone resorption is initiated. This phenomenon is called direct bone resorption.
25  Forces in one direction: orthodontic forces  In the periodontal ligament, zone of compression  zone of tension  temporary increased mobility (functional adaptation ).  no changes in the supracrestal fibres,  no loss of periodontal attachment,  no increased probing pocket depth.  Forces too high (above the adaptation level),  aseptic necrosis of the PDL.  root resorption occurs  resulting in shorter roots.
Tipping movement 26
Bodily movement 27
INDIRECT BONE RESRPTION 28  If the force applied is of higher magnitude, the result may be necrosis of the periodontal ligament tissue in the pressure zone, i.e. decomposition of cells, vessels, matrix, and fi bers (hyalinization). “  Direct bone resorption” therefore cannot occur. Instead, osteoclasts appear in marrow spaces within the adjacent bone tissue where the stress concentration is lower than in the periodontal ligament and a process of undermining or “indirect bone resorption” is initiated.  Through this reaction the surrounding bone is resorbed until there is a breakthrough to the hyalinized tissue within the pressure zone.   Irrespective of whether the bone resorption is of a direct or an indirect nature the tooth moves (tilts) further in the direction of the force.
TRAUMA JIGGLING TYPE 29  Alternate traumatic forces are applied in buccal and lingual directions or mesial and distal directions so that the teeth are not allowed to move away from the force.  There is a combination of pressure and tension zones associated with increased width of the PDL space on both sides, leading to inflammatory changes, active bone resorption and progressive mobility.  (Wentz et al. 1958;Glickman & Smulow 1968; Svanberg & Lindhe 1973; Meitner 1975; Ericsson & Lindhe 1982).  At one stage, when the increasing width reaches a level where it compensates for the forces, the teeth are hypermobile but mobility is no longer progressive
Jiggling type of trauma 30
Healthy periodontium with reduced bone height 31
Periodontitis with reduced bone height 32
33 In presence of plaque-associated periodontal disease, the tissues in the pressure/tension zones could not become adapted and the injury in the zones of co-destruction had a more permanent character.  Continuous alveolar bone destruction  Mobility of the teeth remained progressive  Merging of the zone of irritation and the zone of co-destruction  Dentogingival epithelium proliferated apically and periodontal disease was aggravated.  In conjunction with “jiggling type of trauma” no clear cut pressure and tension sites can be identified but rather there a combination of pressure and tension on both sides of the jiggled tooth
STAGE 11 REPAIR 34  Repair occurs constantly in the normal periodontium, and trauma from occlusion stimulates increased reparative activity.  The damaged tissues are removed, and new connective tissue cells and fibers, bone, and cementum are formed in an attempt to restore the injured periodontium .  Forces remain traumatic only as long as the damage produced exceeds the reparative capacity of the tissues.
Buttressing bone formation 35 Excessive occlusal forces…. resorption of bone…. Body reinforces the thinned bony trabeculae with new bone…Buttressing bone formation CENTRAL Endosteal cells deposit new bone Restores bony trabeculae & reduces the size of marrow spaces PERIPHERAL Shelf like thickening of the alveolar margin LIPPING Bulge in the contour of the facial & lingual bone
Stage III: Adaptive Remodeling of the Periodontium36  If the repair process cannot keep pace with the destruction caused by the occlusion, the periodontium is remodeled in an effort to create a structural relationship in which the forces are no longer injurious to the tissues.  This results in a widened periodontal ligament, which is funnel shaped at the crest, and angular defects in the bone, with no pocket formation. The involved teeth become loose.  Increased vascularization has also been reported
HISTOMETRIC ANALYSIS 37  The three stages in the evolution of traumatic lesions have been differentiated histometrically by the relative amounts of periodontal bone surface undergoing resorption or formation  The injury phase shows an increase in areas of resorption and a decrease in bone formation, whereas the repair phase demonstrates decreased resorption and increased bone formation.  After adaptive remodeling of the periodontium, resorption and formation return to normal.
Relationship Between Plaque-InducedPeriodontal Diseases and Trauma From Occlusion 38  The clinical impressions of early investigators and clinicians assigned an important role to TFO in the etiology of periodontal lesions. Numerous studies have since been performed to determine the mechanisms by which TFO may affect periodontal disease.  These studies can be classified broadly into three categories: -  Human autopsy material  Clinical trials  Animal experiments
HUMAN AUTOPSY MATERIAL 39  Certain criteria were evaluated using human autopsy material. They were  Histopathology of the lesions  Presence of apical extension of microbial deposits  Mobility  Occlusion  Based on these findings, two concepts were proposed: -  Glickmans concept- Theory of Co-destruction.  Waerhaug concept
Glickman’s concept 40  Glickman (1965, 1967) claimed that the pathway of the spread of a plaque-associated gingival lesion can be changed if forces of an abnormal magnitude are acting on teeth harboring subgingival plaque.  Based on this concept, the periodontal structures can be divided into two zones: -  Zone of irritation  Zone of co-destruction Zone of irritation and co-destruction
41  The zone of irritation includes the marginal and interdental gingiva. The soft tissue of this zone is bordered by hard tissue (the tooth) only on one side and is not affected by forces of occlusion.  This means that gingival infl ammation cannot be induced by trauma from occlusion but is the result of irritation from microbial plaque.  The zone of co-destruction includes the periodontal ligament, the root cementum, and the alveolar bone, and is coronally demarcated by the trans-septal (interdental) and the dento-alveolar collagen fi ber bundles . The tissue in this zone may become the seat of a lesion caused by trauma from occlusion.
42  Through this exposure from two different directions the fiber bundles may become dissolved and/or orientated in a direction parallel to the root surface.  The spread of an infl ammatory lesion from the zone of irritation directly down into the periodontal ligament (i.e. not via the interdental bone) may hereby be facilitated  This alteration of the “normal” pathway of spread of the plaque-associated infl ammatory lesion results in the development of angular bony defects.
Waerhaugs concept 43  Waerhaug (1979) examined autopsy specimens similar to Glickman’s, but in addition measured  the distance between the subgingival plaque and  (1) the periphery of the associated infl ammatory cell infi ltrate in the gingiva, and  (2) the surface of the adjacent alveolar bone.  He concluded from his analysis that angular bony defects and infrabony pockets occur equally often at periodontal sites of teeth which are not affected by trauma from occlusion as in traumatized teeth.  In other words, he refuted the hypothesis that trauma from occlusion played a role in the spread of a gingival lesion into the “zone of codestruction”.
44  Loss of connective tissue attachment and the resorption of bone around teeth are exclusively the result of inflammatory lesions associated with subgingival plaque.  Angular bony defects and infrabony pockets occur when the subgingival plaque of tooth has reached a more apical level than the microbiota of the neighboring tooth and the volume of the alveolar bone surrounding the roots is comparatively large.
HUMAN TRIALS 45Rosling et al, 1976: The infrabony pocket located at hypermobile teeth exhibited the same degree healing as those adjacent to firm teeth. Fleszar et al, 1980: Pockets of clinically mobile teeth do not respond as well to periodontal treatment as those of firm teeth exhibiting the same disease activity Richard A. Reinhardt et.al, 1984, used a mathematical system (finite element anaiysis) to calculate principal periodontal ligament stresses in primary and secondary occlusal trauma. The periodontal ligament appears to play a significant role in modulating the stresses transmitted from the root to the bone. Philstrom et al, 1986: teeth with increased mobility and widened PDL space had, in fact, deeper pockets, more attachment loss and less bone support than teeth without these symptoms. Burgett et al: Probing attachment gain was on the average about 0.5mm larger in patients who received scaling and occlusal adjustment than in patients in whom the occlusal adjustment was not included. Neiderud et al, 1992: Tissue alterations which occur at mobile teeth with clinically healthy gingival may reduce the resistance offered by the periodontal tissues to probing. A recent retrospective study (Harrel et al. 2001) showed that: teeth with occlusal discrepancies had deeper PDs and worse prognosis occlusal adjustment improved the prognosis
ANIMAL TRIALS 46  Rochester Group (Polson and co workers)  Used squirrel monkeys  Used mesial-distal compression forces (orthodontic type)  Experimental times up to 10 weeks  Occlusal trauma does not influence periodontal disease progression (No evidence of attachment loss in the presence of plaque and occlusal forces)
47  Gothenburg Group (Lindhe and co workers)  Used beagle dogs  Applied buccal-lingual forces using a cap splint (jiggling type)  Experimental times up to one year  Occlusal trauma could accelerate the progression of periodontal disease (Evidence of attachment loss when plaque and occlusal forces were both present)  This group found that occlusal stresses increase the periodontal destruction induced by periodontitis.
Other theories 48 Trauma from occlusion may alter the pathway of the extension of gingival inflammation to the underlying tissues. This may be favored by the reduced collagen density and the increased number of leukocytes, osteoclasts, and blood vessels in the coronal portion of increasingly mobile teeth. inflammation may then proceed to the periodontal ligament rather than to the bone. Resulting bone loss would be angular, and pockets could become intrabony.  • Trauma-induced areas of root resorption uncovered by apical migration of the inflamed gingival attachment may offer a favorable environment for the formation and attachment of plaque and calculus and therefore may be responsible for the development of deeper lesions. • Supragingival plaque can become subgingival if the tooth is tilted orthodontically or if it migrates into an edentulous area, which results in the transformation of a suprabony pocket into an intrabony pocket.  • Increased mobility of traumatically loosened teeth may have a pumping effect on plaque metabolites, thereby increasing their diffusion.
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52 There is no scientific evidence to show that trauma from occlusion causes gingivitis or periodontitis or accelerates the progression of gingivitis to periodontitis. • The periodontal ligament physiologically adapts to increased occlusal loading by resorption of the alveolar crestal bone, resulting in increased tooth mobility. This is occlusal trauma and is reversible if the occlusal force is reduced. • Occlusal trauma may be a cofactor which can increase the rate of progression of an existing periodontal disease There is a place for occlusal therapy in the management of periodontitis, especially when related to the patient's comfort and function. • Occlusal therapy is not a substitute for conventional methods of resolving plaque-induced inflammation.
MALOCCLUSION ARE TRAUMATIC??? 53 The criterion that determines whether an occlusion is traumatic is whether it produces periodontal injury, not how the teeth occlude. Malocclusion is not necessary to produce trauma; periodontal injury may occur when the occlusion appears normal. Because trauma from occlusion refers to the tissue injury rather than to the occlusion, an increased occlusal force is not traumatic if the periodontium can accommodate it.
EFFECTS OF EXCESSIVE OCCLUSAL FORCESON DENTAL PULP 54  The effects of excessive occlusal forces on the dental pulp have not been established. Some clinicians report the disappearance of pulpal symptoms after the correction of excessive occlusal forces.  Pulpal reactions have been noted in animals subjected to increased occlusal forces, but these did not occur when the forces were minimal and occurred over short periods
PATHOLOGICAL TOOTH MIGRATION 55 Refers to tooth displacement that results when the balance among the factors that maintain physiologic tooth position is disturbed by periodontal disease. may occur in association with gingival inflammation and pocket formation as the disease progresses. most frequently in the anterior region… usually accompanied by mobility and rotation. migration in the occlusal or incisal direction is termed extrusion.
56 Pathogenesis Two major factors play a role in maintaining the normal position of the teeth: 1. Health and normal height of the periodontium and 2. Forces exerted on the teeth. latter includes the forces of occlusion and pressure from the lips, cheeks, and tongue
57 FAILURE TO REPLACE FIRST MOLARS. 1. Second and third molars tilt, resulting in a decrease in vertical dimension 2. PM move distally, and the mandibular incisors tilt or drift lingually. While drifting distally, the mandibular premolars lose their intercuspating relationship with the maxillary teeth and may tilt distally. 3. Anterior overbite is increased. Mandibular incisors strike the maxillary incisors near the gingiva or traumatize the gingiva. 4. The maxillary incisors are pushed labially and laterally 5. The anterior teeth extrude because the incisal apposition has largely disappeared. 6. Diastemata are created by the separation of the anterior teeth
TFO AROUND IMPLANTS 58  An osseointegrated implant is direct contact with the sarrounding bone  It has been suggested that functional load on dental implant may enhance osseointegration and not result in the marginal bone loss when the occlusal load is adequately distributed  But occlusal overload adversly effects the implant stability  It has been suggested by human and animal studies that occlusal overload may cause the loss of osseointegration and early implant failure
Effects of Insufficient Occlusal Force 59  Insufficient occlusal force may also be injurious to the supporting periodontal tissues.  Insufficient stimulation causes thinning of the periodontal ligament, atrophy of the fibers, osteoporosis of the alveolar bone, and a reduction in bone height.  Hypofunction can result from an open-bite relationship, an absence of functional antagonists, or unilateral chewing habits that neglect one side of the mouth
Reversibility of Traumatic Lesions 60  Trauma from occlusion is reversible.  When trauma is artificially induced in experimental animals, the teeth move away or intrude into the jaw.  When the impact of the artificially created force is relieved, the tissues undergo repair.  Although trauma from occlusion is reversible under such conditions, it does not always correct itself, and therefore it is not always temporary or of limited clinical significance.  The injurious force must be relieved for repair to occur.  If conditions in humans do not permit the teeth to escape from or adapt to excessive occlusal force, periodontal damage persists and worsens.  The presence of inflammation in the periodontium as a result of plaque accumulation may impair the reversibility of traumatic lesions.
61  Trauma from occlusion also tends to change the shape of the alveolar crest. The change in shape consists of a widening of the marginal periodontal ligament space, a narrowing of the interproximal alveolar bone, and a shelflike thickening of the alveolar margin.  Therefore although trauma from occlusion does not alter the inflammatory process, it changes the architecture of the area around the inflamed site.  Thus in the absence of inflammation, the response to trauma from occlusion is limited to adaptation to the increased forces.   In the presence of inflammation, however, the changes in the shape of the alveolar crest may be conducive to angular bone loss, and existing pockets may become intrabony.
Diagnosis 62  Cardinal manifestation of  primary TFO is increased tooth mobility.  2. Tilting and migration of individual teeth or of complete segments.  Careful palpation of the muscles of mastication to ascertain whether there is hypertrophy or sign of hypertonicity with possible spasm of one group of muscle  4. Palpation of TMJ and observation of any deviation of the mandible in various paths of closure  5. Fremitus test
MANAGEMENT OF TRAUMA FROM OCCLUSION63  Occlusal Analysis: Occlusion analysis is the study of the relationship of the occlusal surfaces of opposing teeth and their associated functional harmonies  Occlusal registration steps  Occlusal indicator wax  Articulating paper, blue.(40-80 microns)  Occlusal Contact Detection Instruments  Occlusal sonography
DIFFERENT TREATMENT MODALITIES64  Occlusal Adjustment – Coronoplasty  Orthodontic Treatment  Splinting  Temporary  Provisional  Biteplanes
SEQUENCE FOR CORONOPLASTY 65 Step 1: Remove retrusive prematurities and eliminate the deflective shift from RCP to ICP Step 2: Adjust ICP to achieve stable, simultaneous, multipointed, widely distributed contacts. Step 3: Test for excessive contact (fremitus) on the incisor teeth. Step 4: Remove posterior protrusive supracontacts and establish contacts that are bilaterally distributed on the anterior teeth. Step 6: Reduce excessive cusp steepness on the laterotrusive (worki ng) contacts. Step 7: Eliminate gross occlusal disharmonies. Step 8: Recheck tooth contact relationships. Step 9: Polish all rough tooth surfaces
TREATMENT CONSIDERATIONS 66  The goals of the treatment of occlusal traumatism may be described as: 1. elimination or reduction of tooth mobility 2. establishment or maintenance of a stable and reproducible maximal intercuspal habitual position; 3. provision of efficient masticatory function 4. a comfortable occlusion with acceptable phonation and esthetics 5. elimination or modification of parafunctional habits.
67  Treatment of occlusal trauma may be performed at any phase of periodontal therapy.  For chronic periodontitis, treatment efforts are directed toward elimination or minimization of excessive forces, and occlusal therapy may be accomplished through several differentapproaches  occlusal adjustment;  management of parafunctional habits;  temporary, provisional, or long-term stabilization of mobile teeth; orthodontic tooth movement; and occlusal reconstruction or extraction of selected teeth, depending on the case.
68  Treatment of primary or secondary trauma from occlusion requires controlling marginal inflammation and restoring normal occlusal function.  Remission of primary trauma from occlusion proceeds uneventfully if periodontal pockets are successfully treated.  Considering that, treatment of primary trauma from occlusion should basically address the occlusal adjustment to redirect occlusal forces, allowing reversibility of the lesion.  In cases n which periodontitis and trauma from occlusion coexist without producing a combined lesion, treatment should be directed to the independent treatment of both conditions as two distinct pathological entities.  Occlusal adjustment should be performed, when indicated, 45 days prior to periodontal surgery in order to allow rebuilding of existent bone matrix and prevent its loss during surgical debridement of periodontal defects
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CONCLUSION 72  In the field of periodontics, it seems crucial to prevent, treat, and maintain the periodontal supporting apparatus, which is responsible for the long-term stability of teeth.  Accepting this concept, periodontal treatment should be directed at the preservation of periodontal supporting tissues, the homeostatic behavior of which may be dependent on the proper distribution and neutralization of applied mechanical forces.  Most of the research to investigate the role of occlusion in periodontics has been performed in animal models or cadavers and hence does not reflect the real influence of trauma from occlusion in humans.  As a consequence, aggravation of plaque-related inflammatory periodontal disease by trauma from occlusion is still under question, and further investigations are necessaryto elucidate such an association.
REFERENCES 73  Carranza’s Clinical Periodontology; 8th editi; 10 and 13th edition  Clinical Periodontology and Implantology;4th and fifth and 6 thedition; Jan Lindhe  Trauma from Occlusion: The Overstrain of the Supporting Structures of the Teeth Dhirendra Kumar Singh, Md. Jalaluddin, Rajeev Ranjan Indian Journal of Dental Sciences 2017  Role of occlusion in periodontal disease Euloir Passanezi , Adriana Campos Passanezi Sant'Ana Periodontology 2000. 2019;79:129–150.  Trauma from occlusion — An orthodontist’s perspective R. Saravanan, Prajeeth J. Babu, P. Rajakumar Journal of Indian Society of Periodontology - Vol 14, Issue 2, Apr-Jun 2010  Occlusal considerations in periodontics S. J. Davies,1 R. J. M. Gray,2 G. J. Linden,3and J. A. James, BRITISH DENTAL JOURNAL, VOLUME 191, NO. 11, DECEMBER 8 2001

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trauma from occlusion

  • 1.
  • 2.
    CONTENTS  INTRODUCTION  HISTORICALASPECTS  DEFINITIONS  CLASSIFICATION  CLINICAL FEATURES  PERIODONTAL RESPONSE TO EXCESSIVE OCCLUSAL FORCES   INJURY  REPAIR  ADAPTIVE REMODELLING OF THE PERIODONTIUM  TRAUMA FROM OCCLUSION AND PLAQUE-ASSOCIATED PERIODONTAL DISEASE  GLICKMANS’ CONCEPT (THEORY OF CO-DESTRUCTION) WAERHAUG CONCEPT  CLINICAL TRIALS  HUMAN TRIALS  ANIMAL TRIALS  TFO AROUND IMPLANTS  PATHOLOGICAL TOOTH MIGRATION  EFFECT OF TFO ON DENTAL PULP  EFFECETS OF INSUFFICIENT OCCLUSAL FORCES  REVERSIBILITY OF TRAUMATIC LESIONS  LITERATURE REVIEWS  DIAGNOSIS  TREATMENT ASPECTS  CONCLUSION  REFERENCES
  • 3.
    INTRODUCTION  For manyyears, the role of occlusion and its dynamic interactive impact on the periodontium has been an issue of controversy and extensive debate. Although a variety of occlusal conditions have purportedly been related to this interaction, the central focus has been on occlusal trauma resulting from excessive forces applied to the periodontium  Trauma from occlusion is a term used to describe pathologic alterations or adaptive changes which develop in the periodontium as a result of undue force produced by the masticatory muscles.  Trauma from occlusion is only one of many terms that have been used to describe such alterations in the periodontium.  In addition to producing damage in the periodontal tissues, excessive occlusal force may also cause injury in, for example, the temporomandibular joint, the masticatory muscles, and the pulp tissue.
  • 4.
    HISTORICAL ASPECT 4 Karolyi (1901)– Postulated interaction between TFO & “alveolar pyrrohea” Stillman (1917 & 1926) – Advocated use of occlusal adjustment for treatment of TFO Box & Stones (1930’s ) - Animal experiments TFO etiologic factor in periodontal disease Orban & Weinman (1933) - Occlusal forces did not have a major effect on periodontal destruction. Glickman and co- workers (1960s ) - Performed a series of animal model and human autopsy studies Goldman et al in an experimental animal study, evaluated the effects of occlusal trauma on gingival blood flow. Stahl (1968) – Evaluated the interaction between occlusal trauma and plaque-induced periodontal inflammation. Waerhaug (1979)- Evaluated the relationship of the morphology of the bone & pocket with the plaque level and presence or absence of excessive occlusal forces.
  • 5.
    DEFINITIONS 5 Other terms oftenused are: traumatizing occlusion, occlusal trauma, traumatogenic occlusion, periodontal traumatism, overload, etc.  STILLMANN “a condition where injury results to the supporting structures of the teeth by the act of bringing the jaws into a closed position When occlusal forces exceed the adaptive capacity of the tissues, tissue injury results.this resultant injury is termed TFO. (Glickman) STILLMANN “a condition where injury results to the supporting structures of the teeth by the act of bringing the jaws into a closed position Damage in the periodontium caused by stress on the teeth produced directly or indirectly by teeth of the opposing jaw. (WHO,1978) An injury to the attachment apparatus as a result of excessive occlusal force. (Glossary of periodontic terms AAP,1992)
  • 6.
    CLASSIFICATION 6  Glickman’s classification(1953)  According to duration of cause:  i. Acute TFO  ii. Chronic TFO.  According to nature of cause:  i. Primary TFO  ii. Secondary TFO.  Box’s classification  Physiologic occlusion Box defined it as a condition, in which the systems of forces acting upon the tooth during the occlusion are in a state of equilibrium, and they do not and cannot change the normal relationship existing between the tooth and its supporting structures.  Traumatic occlusion The damage produced in the periodontium is due to the overstress produced by the occlusion
  • 7.
    7 •Acute Trauma •Occurs onabrupt occlusal impact. •Caused by restorations or prosthetic appliances that interfere with or alter the direction of occlusal forces on the teeth. •Results in tooth pain, sensitivity to percussion and increased tooth mobility ACUTE TRAUMA •Chronic Trauma •It is more common than acute and is of greater clinical significance. •Caused by gradual changes in the occlusion produced by tooth wear, drifting movement and extrusion of teeth combined with para- functional habits such as bruxism and clenching. CHRONIC TRAUMA
  • 8.
    8 When trauma tothe supporting tissues occurs as a result of alterations in occlusal forces, it is called primary TFO. •High filling •Prosthetic replacement creating excessive forces •Drifting or extrusion of teeth •Orthodontic movement into functionally unacceptable oppositions In primary TFO there are no changes in the level of connective tissue attachment and no pocket formation Secondary TFO Occurs when, the adaptive capacity of the tissues to withstand occlusal forces is impaired by bone loss resulting from marginal inflammation.  This reduces the periodontal attachment area and alters the leverage on the remaining tissues.  The periodontium becomes vulnerable to injury, and previously well tolerated forces become traumatic.  Combined occlusal trauma refers to injury resulting from abnormal occlusal forces applied to a tooth or teeth with inadequate (abnormal) periodontal support
  • 9.
    9  1. Normalperiodontium with normal height of bone  2. Normal periodontium with reduced height of bone  3. Marginal periodontitis with reduced height of bone  It has been found in experimental animals that systemic disorders can reduce tissue resistance and that previously tolerable forces may become excessive. This could theoretically represent another mechanism by which tissue resistance to increased forces is lowered, thereby resulting in secondary trauma from occlusion
  • 10.
    The signs andsymptoms of chronic trauma from occlusion include (AAP, 2000).10  Tooth mobility  Tooth migration  Tooth pain or discomfort on chewing or percussion  Widening of the PDL, disruption of the lamina dura, radiolucency in the furcation or at the apex of vital teeth, root resorption as observed in intra-oral X-rays images  Tenderness of mastication muscles and/or TMJ dysfunction  Presence of wear facets beyond levels expected for patient’s age or diet  Chipped enamel or crown/root factures  Increased width of periodontal ligament space, often with thickening of the lamina dura along the lateral aspect of the root, in the apical and furcation areas,  Angular bone loss, mainly at the coronal level of interdental septum, with a funnel-shaped morphology  Radiolucency lamina dura surrounding the angular bone loss, resembling an infrabony defect  Condensation of the alveolar bone can be produced after widening of the periodontal ligament  Root resorption
  • 11.
    INFLUENCE OF OCCLUSIONON THE PERIODONTIUM11  CLINICAL FEATURES  Progressive mobility  Fremitus  Wear facets  Occlusal discrepencies  Fractured tooth  Thermal sensivity
  • 12.
    12  Fremitus isa measurement of the vibratory patterns of the teeth when the teeth are placed in contacting positions and movements.  A dampened index finger is placed along the buccal and labial surfaces of the maxillary teeth, and patient is asked to tap the teeth together in the maximum ICP and grind systemically in the lateral, protrusive, and lateral protrusive contacting movements and positions  • Class 1: Mild vibration or movement detected  • Class II: Easily palpable vibration but no visible movement  • Class III: Movement visible with the naked eye.
  • 13.
    Radiographic features 13  Increasedwidth of the periodontal space, often with thickening of the lamina dura along the lateral aspect of the root, in the apical region, and in the bifurcation areas.  A vertical destruction of the interdental septum  Root resorption.  Lipping
  • 14.
    Gingival recession?? 14  Althoughit has been speculated that the elimination of trauma by occlusal adjustment, relieving the incidence of excessive occlusal force on teeth showing gingival cleft formation, resulted in spontaneous remission of gingival recession, with no additional treatment performed  Furthermore, no relationship was found between the existence of occlusal discrepancies, whether treated or not, and changes in keratinized gingiva width, as described by Harrel and Nunn  A recent systematic review to investigate the role of traumatic occlusion in the initiation and progression of gingival recessions was performed, in an attempt to gain a clearer understanding of the role of occlusion in these lesions  It could be concluded that the relationship between the conditions remains as “a clinical opinion” and that it seemed convenient to control occlusal factor in clinical practice because it can be considered as an independent risk factor for periodontal disease
  • 15.
    ADAPTIVE CAPACITY OFTHE PERIODONTIUM TO OCCLUSAL FORCES 15 Magnitude : When occlusal force is increased, the periodontium a thickening of the periodontal ligament, an increase in the number and width of the PDL fibers an increase in the density of alveolar bone. 2. Direction : reorientation of the stresses and strains The principal fibers of the PDL are arranged so that they best accommodate occlusal forces along the axis of the tooth . Lateral (horizontal) & torque (rotational) forces more injurious 3. Duration : Constant pressure Intermittent force 4 . Frequency more frequent
  • 16.
    PERIODONTAL RESPONSE TOEXCESSIVE OCCLUSAL FORCES 16  Tissue response occurs in three stages:  Injury  Repair and  Adaptive remodeling of the periodontium
  • 17.
    Tissue injury 17  Tissueinjury is produced by excessive occlusal forces. The body then attempts to repair the injury and restore the periodontium.  This can occur if the forces are diminished or if the tooth drifts away from them. If the offending force is chronic, however, the periodontium is remodeled to cushion its impact.  The ligament is widened at the expense of the bone, which results in angular bone defects without periodontal pockets, and the tooth becomes loose.
  • 18.
    18  Under theforces of occlusion, a tooth rotates around a fulcrum or axis of rotation, which in single-rooted teeth is located in the junction between the middle third and the apical third of the clinical root and in multirooted teeth in the middle of the interradicular bone .  This creates areas of pressure and tension on opposite sides of the fulcrum.  Different lesions are produced by different degrees of pressure and tension. If jiggling forces are exerted, these different lesions may coexist in the same area.
  • 19.
    19  Slightly excessivepressure stimulates resorption of the alveolar bone, with a resultant widening of the periodontal ligament space.  Slightly excessive tension causes elongation of the periodontal ligament fibers and the apposition of alveolar bone.  In areas of increased pressure, the blood vessels are numerous and reduced in size; in areas of increased tension, they are enlarged.
  • 20.
  • 21.
  • 22.
  • 23.
    23  The areasof the periodontium that are most susceptible to injury from excessive occlusal forces are the furcations.  Injury to the periodontium produces a temporary depression in mitotic activity, in the rate of proliferation and differentiation of fibroblasts,in collagen formation, and in bone formation  These return to normal levels after the dissipation of the forces.
  • 24.
    ORTHODONTIC TYPE TRAUMA 24 When a tooth is exposed to unilateral forces of a magnitude, frequency or duration that its periodontal tissues are unable to withstand and distribute while maintaining stability of the tooth, certain well-defined reactions develop in the periodontal structures to the altered functional demand  When horizontally directed forces are applied, the tooth tilts in direction of the force resulting in the development of pressure and tension zones within the marginal and apical parts the tooth becomes hypermobile temporarily, moves to a new position and healing takes place.  If the crown of the tooth is effected by such horizontally directed forces, eventually results in adaptation of periodontal structures to functional demand.  In this tissue reaction, bone resorbing osteoclasts soon appear on the bone surface of the alveolus in the pressure zone. A process of bone resorption is initiated. This phenomenon is called direct bone resorption.
  • 25.
    25  Forces inone direction: orthodontic forces  In the periodontal ligament, zone of compression  zone of tension  temporary increased mobility (functional adaptation ).  no changes in the supracrestal fibres,  no loss of periodontal attachment,  no increased probing pocket depth.  Forces too high (above the adaptation level),  aseptic necrosis of the PDL.  root resorption occurs  resulting in shorter roots.
  • 26.
  • 27.
  • 28.
    INDIRECT BONE RESRPTION 28 If the force applied is of higher magnitude, the result may be necrosis of the periodontal ligament tissue in the pressure zone, i.e. decomposition of cells, vessels, matrix, and fi bers (hyalinization). “  Direct bone resorption” therefore cannot occur. Instead, osteoclasts appear in marrow spaces within the adjacent bone tissue where the stress concentration is lower than in the periodontal ligament and a process of undermining or “indirect bone resorption” is initiated.  Through this reaction the surrounding bone is resorbed until there is a breakthrough to the hyalinized tissue within the pressure zone.   Irrespective of whether the bone resorption is of a direct or an indirect nature the tooth moves (tilts) further in the direction of the force.
  • 29.
    TRAUMA JIGGLING TYPE 29 Alternate traumatic forces are applied in buccal and lingual directions or mesial and distal directions so that the teeth are not allowed to move away from the force.  There is a combination of pressure and tension zones associated with increased width of the PDL space on both sides, leading to inflammatory changes, active bone resorption and progressive mobility.  (Wentz et al. 1958;Glickman & Smulow 1968; Svanberg & Lindhe 1973; Meitner 1975; Ericsson & Lindhe 1982).  At one stage, when the increasing width reaches a level where it compensates for the forces, the teeth are hypermobile but mobility is no longer progressive
  • 30.
  • 31.
    Healthy periodontium withreduced bone height 31
  • 32.
  • 33.
    33 In presenceof plaque-associated periodontal disease, the tissues in the pressure/tension zones could not become adapted and the injury in the zones of co-destruction had a more permanent character.  Continuous alveolar bone destruction  Mobility of the teeth remained progressive  Merging of the zone of irritation and the zone of co-destruction  Dentogingival epithelium proliferated apically and periodontal disease was aggravated.  In conjunction with “jiggling type of trauma” no clear cut pressure and tension sites can be identified but rather there a combination of pressure and tension on both sides of the jiggled tooth
  • 34.
    STAGE 11 REPAIR 34 Repair occurs constantly in the normal periodontium, and trauma from occlusion stimulates increased reparative activity.  The damaged tissues are removed, and new connective tissue cells and fibers, bone, and cementum are formed in an attempt to restore the injured periodontium .  Forces remain traumatic only as long as the damage produced exceeds the reparative capacity of the tissues.
  • 35.
    Buttressing bone formation 35Excessive occlusal forces…. resorption of bone…. Body reinforces the thinned bony trabeculae with new bone…Buttressing bone formation CENTRAL Endosteal cells deposit new bone Restores bony trabeculae & reduces the size of marrow spaces PERIPHERAL Shelf like thickening of the alveolar margin LIPPING Bulge in the contour of the facial & lingual bone
  • 36.
    Stage III: AdaptiveRemodeling of the Periodontium36  If the repair process cannot keep pace with the destruction caused by the occlusion, the periodontium is remodeled in an effort to create a structural relationship in which the forces are no longer injurious to the tissues.  This results in a widened periodontal ligament, which is funnel shaped at the crest, and angular defects in the bone, with no pocket formation. The involved teeth become loose.  Increased vascularization has also been reported
  • 37.
    HISTOMETRIC ANALYSIS 37  Thethree stages in the evolution of traumatic lesions have been differentiated histometrically by the relative amounts of periodontal bone surface undergoing resorption or formation  The injury phase shows an increase in areas of resorption and a decrease in bone formation, whereas the repair phase demonstrates decreased resorption and increased bone formation.  After adaptive remodeling of the periodontium, resorption and formation return to normal.
  • 38.
    Relationship Between Plaque-InducedPeriodontalDiseases and Trauma From Occlusion 38  The clinical impressions of early investigators and clinicians assigned an important role to TFO in the etiology of periodontal lesions. Numerous studies have since been performed to determine the mechanisms by which TFO may affect periodontal disease.  These studies can be classified broadly into three categories: -  Human autopsy material  Clinical trials  Animal experiments
  • 39.
    HUMAN AUTOPSY MATERIAL 39 Certain criteria were evaluated using human autopsy material. They were  Histopathology of the lesions  Presence of apical extension of microbial deposits  Mobility  Occlusion  Based on these findings, two concepts were proposed: -  Glickmans concept- Theory of Co-destruction.  Waerhaug concept
  • 40.
    Glickman’s concept 40  Glickman(1965, 1967) claimed that the pathway of the spread of a plaque-associated gingival lesion can be changed if forces of an abnormal magnitude are acting on teeth harboring subgingival plaque.  Based on this concept, the periodontal structures can be divided into two zones: -  Zone of irritation  Zone of co-destruction Zone of irritation and co-destruction
  • 41.
    41  The zoneof irritation includes the marginal and interdental gingiva. The soft tissue of this zone is bordered by hard tissue (the tooth) only on one side and is not affected by forces of occlusion.  This means that gingival infl ammation cannot be induced by trauma from occlusion but is the result of irritation from microbial plaque.  The zone of co-destruction includes the periodontal ligament, the root cementum, and the alveolar bone, and is coronally demarcated by the trans-septal (interdental) and the dento-alveolar collagen fi ber bundles . The tissue in this zone may become the seat of a lesion caused by trauma from occlusion.
  • 42.
    42  Through thisexposure from two different directions the fiber bundles may become dissolved and/or orientated in a direction parallel to the root surface.  The spread of an infl ammatory lesion from the zone of irritation directly down into the periodontal ligament (i.e. not via the interdental bone) may hereby be facilitated  This alteration of the “normal” pathway of spread of the plaque-associated infl ammatory lesion results in the development of angular bony defects.
  • 43.
    Waerhaugs concept 43  Waerhaug(1979) examined autopsy specimens similar to Glickman’s, but in addition measured  the distance between the subgingival plaque and  (1) the periphery of the associated infl ammatory cell infi ltrate in the gingiva, and  (2) the surface of the adjacent alveolar bone.  He concluded from his analysis that angular bony defects and infrabony pockets occur equally often at periodontal sites of teeth which are not affected by trauma from occlusion as in traumatized teeth.  In other words, he refuted the hypothesis that trauma from occlusion played a role in the spread of a gingival lesion into the “zone of codestruction”.
  • 44.
    44  Loss ofconnective tissue attachment and the resorption of bone around teeth are exclusively the result of inflammatory lesions associated with subgingival plaque.  Angular bony defects and infrabony pockets occur when the subgingival plaque of tooth has reached a more apical level than the microbiota of the neighboring tooth and the volume of the alveolar bone surrounding the roots is comparatively large.
  • 45.
    HUMAN TRIALS 45Rosling etal, 1976: The infrabony pocket located at hypermobile teeth exhibited the same degree healing as those adjacent to firm teeth. Fleszar et al, 1980: Pockets of clinically mobile teeth do not respond as well to periodontal treatment as those of firm teeth exhibiting the same disease activity Richard A. Reinhardt et.al, 1984, used a mathematical system (finite element anaiysis) to calculate principal periodontal ligament stresses in primary and secondary occlusal trauma. The periodontal ligament appears to play a significant role in modulating the stresses transmitted from the root to the bone. Philstrom et al, 1986: teeth with increased mobility and widened PDL space had, in fact, deeper pockets, more attachment loss and less bone support than teeth without these symptoms. Burgett et al: Probing attachment gain was on the average about 0.5mm larger in patients who received scaling and occlusal adjustment than in patients in whom the occlusal adjustment was not included. Neiderud et al, 1992: Tissue alterations which occur at mobile teeth with clinically healthy gingival may reduce the resistance offered by the periodontal tissues to probing. A recent retrospective study (Harrel et al. 2001) showed that: teeth with occlusal discrepancies had deeper PDs and worse prognosis occlusal adjustment improved the prognosis
  • 46.
    ANIMAL TRIALS 46  RochesterGroup (Polson and co workers)  Used squirrel monkeys  Used mesial-distal compression forces (orthodontic type)  Experimental times up to 10 weeks  Occlusal trauma does not influence periodontal disease progression (No evidence of attachment loss in the presence of plaque and occlusal forces)
  • 47.
    47  Gothenburg Group(Lindhe and co workers)  Used beagle dogs  Applied buccal-lingual forces using a cap splint (jiggling type)  Experimental times up to one year  Occlusal trauma could accelerate the progression of periodontal disease (Evidence of attachment loss when plaque and occlusal forces were both present)  This group found that occlusal stresses increase the periodontal destruction induced by periodontitis.
  • 48.
    Other theories 48 Traumafrom occlusion may alter the pathway of the extension of gingival inflammation to the underlying tissues. This may be favored by the reduced collagen density and the increased number of leukocytes, osteoclasts, and blood vessels in the coronal portion of increasingly mobile teeth. inflammation may then proceed to the periodontal ligament rather than to the bone. Resulting bone loss would be angular, and pockets could become intrabony.  • Trauma-induced areas of root resorption uncovered by apical migration of the inflamed gingival attachment may offer a favorable environment for the formation and attachment of plaque and calculus and therefore may be responsible for the development of deeper lesions. • Supragingival plaque can become subgingival if the tooth is tilted orthodontically or if it migrates into an edentulous area, which results in the transformation of a suprabony pocket into an intrabony pocket.  • Increased mobility of traumatically loosened teeth may have a pumping effect on plaque metabolites, thereby increasing their diffusion.
  • 49.
  • 50.
  • 51.
  • 52.
    52 There is noscientific evidence to show that trauma from occlusion causes gingivitis or periodontitis or accelerates the progression of gingivitis to periodontitis. • The periodontal ligament physiologically adapts to increased occlusal loading by resorption of the alveolar crestal bone, resulting in increased tooth mobility. This is occlusal trauma and is reversible if the occlusal force is reduced. • Occlusal trauma may be a cofactor which can increase the rate of progression of an existing periodontal disease There is a place for occlusal therapy in the management of periodontitis, especially when related to the patient's comfort and function. • Occlusal therapy is not a substitute for conventional methods of resolving plaque-induced inflammation.
  • 53.
    MALOCCLUSION ARE TRAUMATIC??? 53 Thecriterion that determines whether an occlusion is traumatic is whether it produces periodontal injury, not how the teeth occlude. Malocclusion is not necessary to produce trauma; periodontal injury may occur when the occlusion appears normal. Because trauma from occlusion refers to the tissue injury rather than to the occlusion, an increased occlusal force is not traumatic if the periodontium can accommodate it.
  • 54.
    EFFECTS OF EXCESSIVEOCCLUSAL FORCESON DENTAL PULP 54  The effects of excessive occlusal forces on the dental pulp have not been established. Some clinicians report the disappearance of pulpal symptoms after the correction of excessive occlusal forces.  Pulpal reactions have been noted in animals subjected to increased occlusal forces, but these did not occur when the forces were minimal and occurred over short periods
  • 55.
    PATHOLOGICAL TOOTH MIGRATION 55 Refersto tooth displacement that results when the balance among the factors that maintain physiologic tooth position is disturbed by periodontal disease. may occur in association with gingival inflammation and pocket formation as the disease progresses. most frequently in the anterior region… usually accompanied by mobility and rotation. migration in the occlusal or incisal direction is termed extrusion.
  • 56.
    56 Pathogenesis Two major factorsplay a role in maintaining the normal position of the teeth: 1. Health and normal height of the periodontium and 2. Forces exerted on the teeth. latter includes the forces of occlusion and pressure from the lips, cheeks, and tongue
  • 57.
    57 FAILURE TO REPLACEFIRST MOLARS. 1. Second and third molars tilt, resulting in a decrease in vertical dimension 2. PM move distally, and the mandibular incisors tilt or drift lingually. While drifting distally, the mandibular premolars lose their intercuspating relationship with the maxillary teeth and may tilt distally. 3. Anterior overbite is increased. Mandibular incisors strike the maxillary incisors near the gingiva or traumatize the gingiva. 4. The maxillary incisors are pushed labially and laterally 5. The anterior teeth extrude because the incisal apposition has largely disappeared. 6. Diastemata are created by the separation of the anterior teeth
  • 58.
    TFO AROUND IMPLANTS 58 An osseointegrated implant is direct contact with the sarrounding bone  It has been suggested that functional load on dental implant may enhance osseointegration and not result in the marginal bone loss when the occlusal load is adequately distributed  But occlusal overload adversly effects the implant stability  It has been suggested by human and animal studies that occlusal overload may cause the loss of osseointegration and early implant failure
  • 59.
    Effects of InsufficientOcclusal Force 59  Insufficient occlusal force may also be injurious to the supporting periodontal tissues.  Insufficient stimulation causes thinning of the periodontal ligament, atrophy of the fibers, osteoporosis of the alveolar bone, and a reduction in bone height.  Hypofunction can result from an open-bite relationship, an absence of functional antagonists, or unilateral chewing habits that neglect one side of the mouth
  • 60.
    Reversibility of TraumaticLesions 60  Trauma from occlusion is reversible.  When trauma is artificially induced in experimental animals, the teeth move away or intrude into the jaw.  When the impact of the artificially created force is relieved, the tissues undergo repair.  Although trauma from occlusion is reversible under such conditions, it does not always correct itself, and therefore it is not always temporary or of limited clinical significance.  The injurious force must be relieved for repair to occur.  If conditions in humans do not permit the teeth to escape from or adapt to excessive occlusal force, periodontal damage persists and worsens.  The presence of inflammation in the periodontium as a result of plaque accumulation may impair the reversibility of traumatic lesions.
  • 61.
    61  Trauma fromocclusion also tends to change the shape of the alveolar crest. The change in shape consists of a widening of the marginal periodontal ligament space, a narrowing of the interproximal alveolar bone, and a shelflike thickening of the alveolar margin.  Therefore although trauma from occlusion does not alter the inflammatory process, it changes the architecture of the area around the inflamed site.  Thus in the absence of inflammation, the response to trauma from occlusion is limited to adaptation to the increased forces.   In the presence of inflammation, however, the changes in the shape of the alveolar crest may be conducive to angular bone loss, and existing pockets may become intrabony.
  • 62.
    Diagnosis 62  Cardinal manifestationof  primary TFO is increased tooth mobility.  2. Tilting and migration of individual teeth or of complete segments.  Careful palpation of the muscles of mastication to ascertain whether there is hypertrophy or sign of hypertonicity with possible spasm of one group of muscle  4. Palpation of TMJ and observation of any deviation of the mandible in various paths of closure  5. Fremitus test
  • 63.
    MANAGEMENT OF TRAUMAFROM OCCLUSION63  Occlusal Analysis: Occlusion analysis is the study of the relationship of the occlusal surfaces of opposing teeth and their associated functional harmonies  Occlusal registration steps  Occlusal indicator wax  Articulating paper, blue.(40-80 microns)  Occlusal Contact Detection Instruments  Occlusal sonography
  • 64.
    DIFFERENT TREATMENT MODALITIES64 Occlusal Adjustment – Coronoplasty  Orthodontic Treatment  Splinting  Temporary  Provisional  Biteplanes
  • 65.
    SEQUENCE FOR CORONOPLASTY 65 Step1: Remove retrusive prematurities and eliminate the deflective shift from RCP to ICP Step 2: Adjust ICP to achieve stable, simultaneous, multipointed, widely distributed contacts. Step 3: Test for excessive contact (fremitus) on the incisor teeth. Step 4: Remove posterior protrusive supracontacts and establish contacts that are bilaterally distributed on the anterior teeth. Step 6: Reduce excessive cusp steepness on the laterotrusive (worki ng) contacts. Step 7: Eliminate gross occlusal disharmonies. Step 8: Recheck tooth contact relationships. Step 9: Polish all rough tooth surfaces
  • 66.
    TREATMENT CONSIDERATIONS 66  Thegoals of the treatment of occlusal traumatism may be described as: 1. elimination or reduction of tooth mobility 2. establishment or maintenance of a stable and reproducible maximal intercuspal habitual position; 3. provision of efficient masticatory function 4. a comfortable occlusion with acceptable phonation and esthetics 5. elimination or modification of parafunctional habits.
  • 67.
    67  Treatment ofocclusal trauma may be performed at any phase of periodontal therapy.  For chronic periodontitis, treatment efforts are directed toward elimination or minimization of excessive forces, and occlusal therapy may be accomplished through several differentapproaches  occlusal adjustment;  management of parafunctional habits;  temporary, provisional, or long-term stabilization of mobile teeth; orthodontic tooth movement; and occlusal reconstruction or extraction of selected teeth, depending on the case.
  • 68.
    68  Treatment ofprimary or secondary trauma from occlusion requires controlling marginal inflammation and restoring normal occlusal function.  Remission of primary trauma from occlusion proceeds uneventfully if periodontal pockets are successfully treated.  Considering that, treatment of primary trauma from occlusion should basically address the occlusal adjustment to redirect occlusal forces, allowing reversibility of the lesion.  In cases n which periodontitis and trauma from occlusion coexist without producing a combined lesion, treatment should be directed to the independent treatment of both conditions as two distinct pathological entities.  Occlusal adjustment should be performed, when indicated, 45 days prior to periodontal surgery in order to allow rebuilding of existent bone matrix and prevent its loss during surgical debridement of periodontal defects
  • 69.
  • 70.
  • 71.
  • 72.
    CONCLUSION 72  In thefield of periodontics, it seems crucial to prevent, treat, and maintain the periodontal supporting apparatus, which is responsible for the long-term stability of teeth.  Accepting this concept, periodontal treatment should be directed at the preservation of periodontal supporting tissues, the homeostatic behavior of which may be dependent on the proper distribution and neutralization of applied mechanical forces.  Most of the research to investigate the role of occlusion in periodontics has been performed in animal models or cadavers and hence does not reflect the real influence of trauma from occlusion in humans.  As a consequence, aggravation of plaque-related inflammatory periodontal disease by trauma from occlusion is still under question, and further investigations are necessaryto elucidate such an association.
  • 73.
    REFERENCES 73  Carranza’s ClinicalPeriodontology; 8th editi; 10 and 13th edition  Clinical Periodontology and Implantology;4th and fifth and 6 thedition; Jan Lindhe  Trauma from Occlusion: The Overstrain of the Supporting Structures of the Teeth Dhirendra Kumar Singh, Md. Jalaluddin, Rajeev Ranjan Indian Journal of Dental Sciences 2017  Role of occlusion in periodontal disease Euloir Passanezi , Adriana Campos Passanezi Sant'Ana Periodontology 2000. 2019;79:129–150.  Trauma from occlusion — An orthodontist’s perspective R. Saravanan, Prajeeth J. Babu, P. Rajakumar Journal of Indian Society of Periodontology - Vol 14, Issue 2, Apr-Jun 2010  Occlusal considerations in periodontics S. J. Davies,1 R. J. M. Gray,2 G. J. Linden,3and J. A. James, BRITISH DENTAL JOURNAL, VOLUME 191, NO. 11, DECEMBER 8 2001

Editor's Notes

  • #5 Karolyi was the first one to start the most controversial issue by introducing in 1901 the concept of bruxism as a significant factor in the pathogenesis of periodontitis. It is known as the “Karolyi effect the first comprehensive study of the role of occlusal stress on teeth in relation to periodontal disease was made by Talbot, who pointed out that man is predisposed to disease of the supporting tissues of the teeth because jaw function has been greatly decreased by modern methods of food preparation. Box et al. did study on sheeps’ tooth suggesting that TFO produces vertical bone defect. Stillman[8] was the first toemphasize traumatic occlusion as a cause of periodontaldisease. Repeated abnormal pressures of one tooth on anotherproduce traumatic injury. He pointed out that there arenoninfectious changes that are directly produced by traumaticocclusion. Glickman and Smulow[9‑11] proposed the theory in the early1960s that a traumatogenic occlusion could act as a cofactor inthe progression of periodontitis. This theory is known as the “codestructive theory.” Goldman[12] proved that occlusal traumawas not the cause of soft tissue lesions such as Stillman’s clefts and McCall’s festoons Waerhaug[13,14] proved the involvement of TFO in the pathogenesis of Infrabony pockets. Polson[15,16] used squirrel monkeys as their animal model. Houston et al.[17] concluded that there is no correlation between periodontal disease and bruxism; they seldom occurred in the same individual, and bruxism and occlusal status are not closely associated. Burgett et al.[18] found no significant difference in the in tooth mobility between the adjusted and the nonadjustedgroups. Wolffe et al.[19] stated that “a periodontium remained healthy despite the persistent forces that caused the drifting of the teeth and significant changes in occlusion Ericsson et al.[20] showed that splinting failed to retard attachment loss or to inhibit plaque down growth. He showed that despite healthy gingival tissues, jiggled teeth lost marginal bone and had more probing depth when compared to the nonjiggled.
  • #12 Cardinal manifestation of primary TFO is increased tooth mobility. The mobility can be assessed by mechanical and electronic instrument Increased mobility is seen in two conditions: Destruction of periodontal fibers in the injury stage Widening of the PDL space in the final phase PERIOTEST , PERIODONTOMETER Occlusal or incisal surface worn out by attrition is called facet. When active tooth gnashing occurs, the enamel rods are fractured and become highly reflective to light. Thus curvy, smooth, and curviplanar facets are indicative of ongoing frictional activity. Facets can be classified into two types: Horizontal facets Vertical facets
  • #16 Changes in the periodontium depend on the magnitude, direction, duration, and frequency of increased occlusal forces. When the magnitude of occlusal forces is increased, the periodontium responds with a widening of the periodontal ligament space, an increase in the number and width of periodontal ligament fibers, and an increase in the density of alveolar bone. Changing the direction of occlusal forces causes a reorientation of the stresses and strains within the periodontium (Fig. 25.1).23 The principal fibers of the periodontal ligament are arranged so that they best accommodate occlusal forces along the long axis of the tooth. Lateral (horizontal) and torque (rotational) forces are more likely to injure the periodontium. The response of alveolar bone is also affected by the duration and frequency of occlusal forces. Constant pressure on the bone is more injurious than intermittent forces. The more frequent the application of an intermittent force, the more injurious the force is to the periodontium FIG.
  • #21 Greater pressure produces a gradation of changes in the periodontal ligament, starting with compression of the fibers, which produces areas of hyalinization.54-56 Subsequent injury to the fibroblasts and other connective tissue cells leads to necrosis of areas of the ligament.52,56 Vascular changes are also produced: within 30 minutes, impairment and stasis of blood flow occur; at 2 to 3 hours, blood vessels appear to be packed with erythrocytes, which start to fragment; and between 1 and 7 days, disintegration of the blood vessel walls and release of the contents into the surrounding tissue occur.53,63 In addition, increased resorption of alveolar bone and resorption of the tooth surface occur
  • #22 Severe tension causes widening of the periodontal ligament, thrombosis, hemorrhage, tearing of the periodontal ligament, and resorption of alveolar bone.
  • #23 Pressure severe enough to force the root against bone causes necrosis of the periodontal ligament and bone. The bone is resorbed from viable periodontal ligament adjacent to necrotic areas and from marrow spaces; this process is called undermining resorption.
  • #25 These studies involved the placement of high crowns or restorations on the teeth of dogs or monkeys, resulting in a continuous or intermittent force in one direction.
  • #29 This breakthrough results in a reduction of the stress in this area, and cells from the neighboring bone or adjacent areas of the periodontal ligament can proliferate into the pressure zone and replace the previously hyalinized tissue, thereby re-establishing prerequisites for “direct bone resorption”.
  • #30 Trauma from occlusion in humans, however, occurs as a result of forces that act alternatively in opposite directions. These were analyzed in experimental animals with jiggling forces, usually produced by means of a high crown combined with an orthodontic appliance. In another method, the teeth were separated by wooden or elastic material wedged interproximally to displace a tooth toward the opposite proximal side. After 48 hours the wedge was removed, and the procedure repeated on the opposite side
  • #36 When bone is resorbed by excessive occlusal forces, the body attempts to reinforce the thinned bony trabeculae with new bone (Fig. 25.6). This attempt to compensate for lost bone is called buttressing bone formation, and it is an important feature of the reparative process associated with trauma from occlusion.16 It also occurs when bone is destroyed by inflammation or osteolytic tumors. Buttressing bone formation occurs within the jaw (central buttressing) and on the bone surface (peripheral buttressing). During central buttressing, the endosteal cells deposit new bone, which restores the bony trabeculae and reduces the size of the marrow spaces. Peripheral buttressing occurs on the facial and lingual surfaces of the alveolar plate. Depending on its severity, peripheral buttressing may produce a shelflike thickening of the alveolar margin, which is referred to as lipping (Fig. 25.7), or a pronounced bulge in the contour of the facial and lingual bone
  • #38 Evolution of traumatic lesions as depicted experimentally in rats by variations in relative amounts of areas of bone formation and bone resorption in periodontal bone surfaces. The horizontal axis shows the number of days after the initiation of traumatic interference. The vertical axis shows the percentage of bone surface undergoing resorption or formation. The stages in the evolution of the lesions are represented in the top drawings, which show the average amount of bone activity for each group
  • #39 The clinical impressions of early investigators and clinicians assigned an important role to trauma from occlusion in the etiology of periodontal lesions. Since then, numerous studies have been performed that have attempted to determine the mechanisms by which trauma from occlusion may affect periodontal disease The interaction between trauma from occlusion and plaque-associated periodontal disease in humans was frequently discussed in the period 1955–1970
  • #42 estruction from the zone of irritation can be affected from two different directions: 1. From the infl ammatory lesion maintained by plaque in the zone of irritation 2. From trauma-induced changes in the zone of co-destruction.
  • #43 bundles. It is the seat of a lesion caused by trauma from occlusion. The fiber bundles which separate the zone of co-destruction from the zone of irritation can be affected from two different directions: - from the inflammatory lesion maintained by plaque in the zone of irritation from trauma induced changes in the zone of co-destruction Alteration of the normal pathway of spread results in development of angular bony defects
  • #44  (Fig. 14-1): The periodontal structures can be divided into two zones1. The zone of irritation 2. The zone of co-destruction.
  • #45 Waerhaug’s observations support findings presented by Prichard (1965) and Manson (1976) which imply that the pattern of loss of supporting structures is the result of an interplay between the form and volume of the alveolar bone and the apical extension of the microbial plaque on the adjacent root surfaces
  • #47 The Eastman Dental Center group in Rochester, New York, used squirrel monkeys, produced trauma by repetitive interdental wedging, and added mild to moderate gingival inflammation; experimental times were up to 10 weeks. They reported that the presence of trauma did not increase the loss of attachment induced by periodontitis.42,45
  • #48 The University of Gothenburg group in Sweden used beagle dogs, produced trauma by placing cap splints and orthodontic appliances, and induced severe gingival inflammation; experimental times were up to 1 year.
  • #53 By analyzing data from the literature, several points were stressed by the authors, including
  • #54 Any occlusion that produces periodontal injury is traumatic. Malocclusion is not necessary to produce trauma; periodontal injury may occur when the occlusion appears normal. The dentition may be anatomically and aesthetically acceptable but functionally injurious. Similarly, not all malocclusions are necessarily injurious to the periodontium
  • #57 Tooth with weakened support….unable to maintain its normal position in the arch and moves away from the opposing force unless it is restrained by proximal contact. Force that moves the weakly supported tooth……created by factors such as occlusal contacts or pressure from the tongue. Changes in the Forces Exerted on the Teeth Changes in the magnitude, direction, or frequency of the forces exerted on the teeth can induce pathologic migration of a tooth or group of teeth. Changes in the forces may occur as a result of unreplaced missing teeth, failure to replace first molars, or other causes
  • #64 The primary purpose of occlusion analysis is to reveal interferences in articulation which cannot be observed directly in the mouth. Once the simple diagnostic casts are transferred to an adjustable articulator via face bow and bite fork.
  • #66 retruded cuspal position (RCP) to intercuspal position (ICP